• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Epigallocatechin-3-O-gallate Decreases Tumor Necrosis Factor-alpha-induced Fractalkine Expression in Endothelial Cells by Suppressing NF-kappa B
【24h】

Epigallocatechin-3-O-gallate Decreases Tumor Necrosis Factor-alpha-induced Fractalkine Expression in Endothelial Cells by Suppressing NF-kappa B

机译：Epigallocatechin-3-O-gallate通过抑制NF-κB降低肿瘤坏死因子-α诱导的Fractalkine在内皮细胞中的表达。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Epigallocatechin-3-O-gallate (EGCG), the main catechin in green tea, has anti-oxidant, anti-atherosclerotic and anti-inflammatory properties. Fractalkine, a chemokine involved in inflammation and early atherosclerotic processes, acts as a chemoattractant as well as an adhesion molecule in endothelial cells activated by proinflammatory cytokines. In the present study, we investigated the effect of EGCG on fractalkine expression in TNF-alpha-induced human umbilical vein endothelial cells (HUVECs). EGCG decreased TNF-alpha-induced fractalkine mRNA and protein expression in HUVECs in a time-dependent manner. EGCG suppressed the TNF-a-induced phosphorylation and degradation of I kappa B-alpha, thereby decreasing the phosphorylation and nuclear translocation of the NF-kappa B p65 subunit in HUVECs. The DNA binding activity of the NF-kappa B p65 subunit was lower in EGCG-pretreated HUVECs than in those treated with TNF-alpha alone. Furthermore, EGCG inhibited monocyte adhesion to HUVECs stimulated by TNF-alpha. The silencing of fractalkine with an siRNA or treatment with a blocking antibody against fractalkine suppressed the TNF-alpha-induced increase in monocyte adhesion. These results demonstrate that EGCG prevents TNF-alpha-induced vascular endothelial fractalkine expression.
机译：Epigallocatechin-3-O-gallate（EGCG）是绿茶中的主要儿茶素，具有抗氧化，抗动脉粥样硬化和消炎的特性。 Fractalkine是一种参与炎症和早期动脉粥样硬化过程的趋化因子，在促炎性细胞因子激活的内皮细胞中起趋化作用以及粘附分子的作用。在本研究中，我们调查了EGCG对TNF-α诱导的人脐静脉内皮细胞（HUVECs）中fractalkine表达的影响。 EGCG以时间依赖性方式降低HUVEC中TNF-α诱导的fractalkine mRNA和蛋白表达。 EGCG抑制TNF-a诱导的IκB-α的磷酸化和降解，从而降低HUVEC中NFκB p65亚基的磷酸化和核易位。在EGCG预处理过的HUVEC中，NF-κBp65亚基的DNA结合活性比单独用TNF-α处理的低。此外，EGCG抑制了单核细胞与TNF-α刺激的HUVEC的粘附。用siRNA沉默fractalkine或用针对fractalkine的封闭抗体处理可抑制TNF-α诱导的单核细胞粘附增加。这些结果表明，EGCG可以阻止TNF-α诱导的血管内皮分数链烷烃表达。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号